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Subversion of the host cell cytoskeleton and innate immunity by Chlamydia trachomatis

Award Number: F32AI138372
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 04/01/2019
PERIOD OF PERFORMANCE END DATE: 09/30/2022

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Subversion of the host cell cytoskeleton and innate immunity by Chlamydia trachomatis - Abstract Background: The Gram-negative obligate intracellular bacterium Chlamydia trachomatis infects epithelia of the urogenital tract causing tissue damage, pelvic inflammatory disease and infertility. Chlamydiae utilize a type III secretion (T3S) system to deliver a network of effectors to host epithelial cells to establish an infection. How the T3S effectors subvert the host cell machinery and regulate the innate immune response is poorly understood. Broad, long-term objective: The objective of this proposal is to define at the molecular level how a network of Chlamydia effectors delivered during early infection regulate the host epithelial cell cytoskeleton, tissue architecture and the innate immune response in a novel three-dimensional endometrial organoid (EO) system. This new infection model is ideal for studying Chlamydia infection – fully differentiated and diverse polarized epithelia positioned in a 3D environment, which mimics tissue architecture in vivo and betters recapitulates the organization of the cytoskeleton and interaction with immune cells. Specific aims: Aim 1 of this study is to functionally characterize the EO infection model, examine how the T3S effector TepP affects epithelial integrity and immune cell recruitment, and define cell-type-specific responses to infection. Aim 2 investigates how an early T3S effector network cooperatively subverts host cell signaling pathways to promote inclusion biogenesis, maturation and bacterial replication. Method: I will combine a targeted gene disruption technique using group II intronic insertion to generate Chlamydia T3S effector deficient strains, a three-dimensional organoid infection model, immune cell recruitment assays, and high-resolution light microscopy. Biochemical techniques including affinity purification coupled to mass-spectrometry will identify host targets of T3S effectors. Health-relatedness: Chlamydia infections are the leading cause of preventable blindness in the developing world and the most common sexually transmitted bacterial pathogen. Repeated infections lead to chronic immune cell infiltration that can result in tissue scarring and damage. Significantly, infections can lead to severe sequelae and are associated with cervical and ovarian cancer, yet the mechanisms by which Chlamydia disrupts epithelial tissue structure, function and growth are poorly understood. The proposed research utilizes cutting-edge infection models and new genetic techniques to understand how Chlamydia virulence factors target host cell factors to disrupt epithelial tissue functions and regulate the innate immune response.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2023 ( Subtotal = $0 )
2023	2021	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Allergy and Infectious Diseases Research	000	3	7/21/2023	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2021 ( Subtotal = $105,687 )
2021	2021	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	000	3	3/23/2021	NON-COMPETING CONTINUATION	$70,458
2021	2021	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	001	3	9/7/2021	SUPPLEMENT FOR EXPANSION	$35,229
2021	2021	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	002	3	9/8/2021	NON-COMPETING CONTINUATION	$0
														Subtotal = $105,687

Issue Date FY: 2020 ( Subtotal = $67,446 )
2020	2020	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	000	2	3/20/2020	NON-COMPETING CONTINUATION	$67,446
														Subtotal = $67,446

Issue Date FY: 2019 ( Subtotal = $61,610 )
2019	2019	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	003	1	11/29/2018	NEW	$0
2019	2019	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	002	1	11/29/2018	NEW	$2,572
2019	2019	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	000	1	10/30/2018	NEW	$59,038
2019	2019	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	001	1	11/5/2018	NEW	$0
2019	2019	DUKE UNIVERSITY	2200 W MAIN ST STE 710	DURHAM	NC	27708	DURHAM	USA	Allergy and Infectious Diseases Research	004	1	12/27/2018	NEW	$0
														Subtotal = $61,610

Grand Total All Awards = $234,743

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Subversion of the host cell cytoskeleton and innate immunity by Chlamydia trachomatis

Award Number: F32AI138372

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 04/01/2019

PERIOD OF PERFORMANCE END DATE: 09/30/2022

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